A large‐scale survey study was conducted to assess trauma, burnout, posttraumatic growth, and associated factors for nurses in the COVID‐19 pandemic. The Trauma Screening Questionnaire, Maslach Burnout Inventory, and Posttraumatic Growth Inventory‐Short Form were utilized. Factors associated with trauma, burnout, and posttraumatic growth were analysed using logistic and multiple regressions. In total, 12 596 completed the survey, and 52.3% worked in COVID‐19 designated hospitals. At the survey’s conclusion in April, 13.3% reported trauma (Trauma ≥ 6), there were moderate degrees of emotional exhaustion, and 4,949 (39.3%) experienced posttraumatic growth. Traumatic response and emotional exhaustion were greater among (i) women (odds ratio [OR]: 1.48, 95% CI 1.12–1.97 P = 0.006; emotional exhaustion OR: 1.30, 95% CI 1.09–1.54, P = 0.003), (ii) critical care units (OR: 1.20, 95% CI 1.06–1.35, P = 0.004; emotional exhaustion OR: 1.23, 95% CI 1.12–1.33, P < 0.001) (iii) COVID‐19 designated hospital (OR: 1.24, 95% CI 1.11–1.38; P < 0.001; emotional exhaustion OR: 1.26, 95% CI 1.17–1.36; P < 0.001) and (iv) COVID‐19‐related departments (OR: 1.16, 95% CI 1.04–1.29, P = 0.006, emotional exhaustion only). To date, this is the first large‐scale study to report the rates of trauma and burnout for nurses during the COVID‐19 pandemic. The study indicates that nurses who identified as women, working in ICUs, COVID‐19 designated hospitals, and departments involved with treating COVID‐19 patients had higher scores in mental health outcomes. Future research can focus on the factors the study has identified that could lead to more effective prevention and treatment strategies for adverse health outcomes and better use of resources to promote positive outcomes.

Fas ligand (CD95L) inhibits T cell function in immune-privileged organs such as the eye and testis, yet in most tissues CD95L expression induces potent inflammatory responses. With a stably transfected colon carcinoma cell line, CT26-CD95L, the molecular basis for these divergent responses was defined. When injected subcutaneously, rejection of CT26-CD95L was caused by neutrophils activated by CD95L. CT26-CD95L survived in the intraocular space because of the presence of transforming growth factor-beta (TGF-beta), which inhibited neutrophil activation. Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection.

Dendritic cell (DC)-based antitumor vaccine is a novel cancer immunotherapy that is promising for reducing cancer-related mortality. However, results from early clinical trials were suboptimal. A possible explanation is that many tumors secrete immunosuppressive factors such as TGF-β, which may hamper host immune response to DC vaccine. In this study, we demonstrated that TGF-β produced by tumors significantly reduced the potency of DC/tumor fusion vaccines. TGF-β-secreting (CT26-TGF-β) stable mouse colon cancer cell lines were generated using a retroviral vector expressing TGF-β. A non-TGF-β-secreting (CT26-neo) cell line was generated using an empty retroviral vector. The efficacies of DC/tumor fusion vaccines were assessed in vitro and in vivo. DC/CT26-TGF-β fusion cells failed to induce a strong T cell proliferative response in vitro, mainly due to the effect of TGF-β on T cell responsiveness rather than DC stimulatory capability. Animals vaccinated with DC/CT26-TGF-β fusion vaccine had lower tumor-specific CTL activity and had significantly lower survival after tumor challenge as compared with animals immunized with DC/CT26-neo hybrids (45 vs 77%, p &lt; 0.05). Ex vivo exposure of DCs to TGF-β did not appear to lessen the efficacy of DC vaccine. These data suggest that tumor-derived TGF-β reduces the efficacy of DC/tumor fusion vaccine via an in vivo mechanism. Neutralization of TGF-β produced by the fusion cells may enhance the effectiveness of DC-based immunotherapy.